Poor growth of the fetus in utero, or intrauterine growth restriction (IUGR), increases visceral obesity and associated co-morbidities in humans. Visceral obesity is associated with increased expression of the PPAR? gene. Expression of genes is controlled by epigenetics and one epigenetic modifying enzyme is Setd8. We showed in other tissue types that Setd8 affects PPAR? epigenetics in association with changes in PPAR? expression. However, it is unknown if 1) this occurs in visceral adipose tissue, 2) if it is affected by IUGR, or 3) if the PPAR? -setd8 and PPAR? expression are causatively related. This proposal uses a rat model of IUGR to understand the relationship between IUGR and PPAR? -Setd8-epigentics in the adipose tissue. We will test two hypotheses in this proposal. First, that increased Setd8 levels in male IUGR rat visceral adipose tissue are associated with increased levels of an epigenetic modification made by Setd8, H4K20Me, of the PPAR? gene. For this we will use a rat model of IUGR. Second, we will test the hypothesis that IUGR increases lipid uptake by primary visceral adipose culture while knockdown of Setd8 or PPAR? reduces lipid uptake, PPAR?2 expression and H4K20Me of the PPAR? gene. To test this, we will use primary adipose cell culture. This work is significant to public health because understanding one molecular mechanism by which IUGR induces epigenetic modifications to PPAR? in IUGR visceral adipose tissue will provide insight into the root causes of visceral obesity in IUGR. Understanding these mechanisms will lead to the ability to develop interventions that can target specific epigenetic changes, with the potential to improve the metabolic health of formally growth restricted individuals.